Neuronal-glial interactions are implicated in normal information processing, neuroprotection, and modulation of neuronal activity including rate of spontaneous firing and threshold of activation. It is generally believed that inflammatory and neuropathic pain are an expression of neural plasticity, which can occur as both peripheral sensitization, an increase in the sensitivity and excitability of primary sensory neurons in the peripheral nervous system (PNS), and central sensitization, an increase in the activity and excitability of nociceptive neurons in the spinal cord and brain in the central nervous system (CNS) that leads to the development and maintenance of chronic pain (Ji et al., Trends in Neurosciences. 26 (12):696-705 (2003); Julius D. & Basbaum A. I., Nature. September 13; 413 (6852):203-10 (2001); Woolf C. J. & Salter M. W., Science. 2000 June 9; 288 (5472):1765-9; Latremoliere A. & Woolf C. J. The Journal of Pain. 2009 September; 10 (9):895-926). In recent years, it is increasingly recognized that glial cells in the PNS (e.g., Schwann cells and satellite cells) and CNS (e.g., astrocytes and microglia) play a critical role in chronic pain processing by modulating neuronal excitability (Ji et al., Neuron Glia Biology. 2006 November; 2 (4):259-69; McMahon S B & Malcangio M., Neuron. 2009 Oct. 15; 64 (1):46-54; Milligan E D & Watkins L R, Nature Reviews Neuroscience. 2009 January; 10 (1):23-36; Romero-Sandoval A et al., Brain Research. 2008 July 11; 1219: 116-126; Scholz J & Woolf C J. Nat Neuroscience. 2007 November; 10 (11):1361-8). Nerve injury or activation of sensory neurons in response to inflammatory stimuli induces substantial changes in both microglia and astrocytes in the spinal cord (DeLeo J A et al., Neuroscientist. 2004 February; 10 (1):40-52; Jin S X et al., Journal of Neuroscience. 2003 May 15; 23 (10):4017-22; Zhuang Z Y et al., Journal of Neuroscience. 2006 Mar. 29; 26 (13):3551-60). Furthermore, data from studies of glial inhibition support an important role of spinal microglia and astrocytes in enhancing inflammatory and neuropathic pain. It is generally believed that spinal glial cells enhance and maintain inflammatory and neuropathic pain by releasing potent neuromodulators, such as proinflammatory cytokines, chemokines, and growth factors (Abbadie C. Trends in Immunology. 2005 October; 26 (10):529-34; Abbadie C. et al., Brain Research Reviews. 2009 April; 60 (1):125-34; Gao Y J et al., Journal of Neuroscience. 2009 Apr. 1; 29 (13):4096-108; Inoue E. et al., Neuron. 2006 Apr. 20; 50 (2):261-75; Milligan E D & Watkins L R, Nature Reviews Neuroscience. 2009 January; 10 (1):23-36; Trang T. et al., Journal of Neuroscience. 2009 Mar. 18; 29 (11):3518-28; Watkins L R & Maier S F. Physiological Reviews. 2002 October; 82 (4):981-1011; White F A & Wilson N M, Current Opinion in Anesthesiology. 2008 October; 21 (5):580-5)).